Cases reported "Hyponatremia"

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1/37. Hyponatraemia associated with lamotrigine in cranial diabetes insipidus.

    We report the cases of two children with cranial diabetes insipidus who were treated with lamotrigine for seizures and who had accompanying changes in desmopressin requirements. Lamotrigine is a new anticonvulsant chemically unrelated to other existing antiepileptic drugs. Studies suggest it acts at voltage-sensitive sodium channels and also decreases calcium conductance. Both of these mechanisms of action are shared by carbamazepine, which can cause hyponatraemia secondary to inappropriate secretion of antidiuretic hormone. It is possible that the effect of lamotrigine on fluid balance in the cases described is also centrally mediated.
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keywords = diabetes insipidus, insipidus, diabetes
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2/37. Cerebral oedema in enuretic children during low-dose desmopressin treatment: a preventable complication.

    Seven cases of cerebral oedema have been observed in enuretic children during low-dose desmopressin (DDAVP) treatment given in a dose of 7-21 microg daily in the czech republic between 1995 and 1999, after the drug started to be marketed for this indication and delivered in simple bottles with a dropper. All seven children (age 5-11 years, four boys) experienced a period of unconsciousness but all recovered without sequelae. In most cases, safety measures were underestimated and natraemia was not regularly controlled. Two children developed cerebral oedema after excessive water intake in preparation for uroflowmetry, another one drank much during a hot summer day, in one diabetes insipidus was not recognised and two children were clearly non-compliant with reduced fluid intake on a long-term basis. Only in one child, no risk factor was found. Conclusion. Proper selection and instruction of patients is needed to avert cerebral oedema during treatment with desmopressin for nocturnal enuresis.
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ranking = 0.2
keywords = diabetes insipidus, insipidus, diabetes
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3/37. hyponatremia and polyuria in children with central diabetes insipidus: challenges in diagnosis and management.

    Five patients with well-controlled, long-standing, central diabetes insipidus had acute development of dehydration, hyponatremia, and inappropriate natriuresis in the setting of polyuria resistant to exogenous antidiuretic hormone. hyponatremia and dehydration worsened with fluid restriction or use of exogenous antidiuretic hormone. We discuss the challenges in diagnosis and management of probable salt wasting in children with central diabetes insipidus.
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ranking = 1.2
keywords = diabetes insipidus, insipidus, diabetes
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4/37. Sodium and water disturbances in patients with Sheehan's syndrome.

    Sheehan's syndrome has been attributed to ischemic damage of the pituitary gland or hypothalamic-pituitary stalk during the peripartum period. Well-described clinical features of Sheehan's syndrome include hypothyroidism, adrenal insufficiency, hypogonadism, growth hormone deficiency, hypoprolactinemia, and different sodium and water disturbances. The occurrence of sodium and water disturbances associated with Sheehan's syndrome depends on the degree of pituitary damage, time of onset since the initial pituitary insult, and concurrent medical conditions that also may play a role in sodium and water balance. We present a patient with Sheehan's syndrome with severe chronic hyponatremia; discuss a potential problem in the patient's management; and review the literature for various sodium and water disturbances, including acute and chronic hyponatremia as well as overt and subclinical central diabetes insipidus. Although Sheehan's syndrome is more prevalent in developing countries, the increasingly large immigrant population within the united states warrants better awareness of this syndrome and its potential complicating sodium and water disturbances. Prompt diagnosis and an understanding of the pathogenic mechanisms of sodium and water disturbances associated with Sheehan's syndrome may avoid potential treatment-related complications.
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ranking = 0.2
keywords = diabetes insipidus, insipidus, diabetes
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5/37. hyponatremia associated with desmopressin for the treatment of nocturnal polyuria.

    Desmopressin diacetate arginine vasopressin (DDAVP) is a synthetic analogue of the mammalian arginine vasopressin used in the treatment of central diabetes insipidus, bleeding disorders, and incontinence. The primary adverse reaction associated with DDAVP is hypotonic hyponatremia. hyponatremia has been reported in adults treated with DDAVP for Von Willebrand's disease and hemophilia and in children treated for enuresis, but as yet few cases of hyponatremia developing in enuretic adults treated with DDAVP have been reported. We report the cases of two elderly women taking DDAVP for nocturnal polyuria who developed severe hyponatremia. One patient died in the hospital.
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ranking = 0.2
keywords = diabetes insipidus, insipidus, diabetes
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6/37. Rathke's cleft cyst presenting with hyponatremia and transient central diabetes insipidus.

    We describe an 18-year-old female who complained of general weakness, nausea, vomiting, headache, and lightheadedness. On physical examination, she was euvolemic without visual or neurological deficits. The striking biochemical abnormality was hyponatremia (125 mmol/l). This hyponatremia met the laboratory diagnostic criteria for the syndrome of inappropriate secretion of antidiuretic hormone (SIADH). Two litres of normal saline were given per day for 4 days and this did not correct her hyponatremia. A spontaneous diuresis (6.6 l) developed in 1 day, causing a rise in her PNa of 26 mmol and a final PNa of 152 mmol/l. magnetic resonance imaging revealed a dumbell-shaped intrasellar and suprasellar cyst. During transsphenoidal surgery, a Rathke's cleft cyst (RCC) lined with columnar epithelium containing mucoid material was resected. We speculate that the growing RCC may have produced critical compression over the stalk, thus contributing to the transition from SIADH with hyponatremia to transient central diabetes insipidus with hypernatremia.
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keywords = diabetes insipidus, insipidus, diabetes
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7/37. Cortical blindness after contrast-enhanced CT: complication in a patient with diabetes insipidus.

    Transient cortical blindness is an uncommon but well-known complication following cerebral angiography. One possible cause of this complication is an adverse reaction to contrast agent, resulting in an osmotic disruption of the blood-brain barrier that seems to be selective for the occipital cortex. We report the case of a 16-year-old male patient with cortical blindness after intravenous application of nonionic contrast agent during CT angiography performed because of seizure that was attributed to thrombosis of the basilar artery on the basis of clinical findings. To our knowledge, the development of cortical blindness after CT angiography has not been described in the literature. The patient's symptoms were triggered by hyponatriemia and diabetes insipidus.
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keywords = diabetes insipidus, insipidus, diabetes
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8/37. Transient hyponatremia after damage to the neurohypophyseal tracts.

    Section of the neurohypophyseal stalk classically produces a triphasic response: diabetes insipidus (1st phase), hyponatremia or normonatremia (2nd phase), and diabetes insipidus (3rd phase). Transient hyponatremia without diabetes insipidus has been reported after transsphenoidal pituitary surgery. We report two additional cases of transient hyponatremia which occurred 6-8 days after pituitary surgery. We hypothesize that this outcome may be due to partial section or damage of the hypothalamiconeurohypophyseal tracts. The remaining intact vasopressin neurons function normally to protect against the diabetes insipidus of the first and third phase, but leak of vasopressin from the damaged tracts and posterior pituitary is sufficient to cause what can be described as an isolated second phase. To study this hypothesis in rats, partial damage to the hypothalamicneurohypophyseal tracts was produced by radiofrequency lesions. The lesions did not affect anterior pituitary function. A variety of responses in posterior pituitary function occurred, including classic triphasic response in 2 rats and transient hyponatremia in 20 of 35 lesioned animals. The mean sodium nadir was 128.7 /- 1.5 mEq/l in comparison to the sham-operated value of 140.0 /- 0.4 mEq/l. Of the 20 rats exhibiting transient hyponatremia, 12 went on to develop diabetes insipidus, and 8 recovered. In the recovered group, the transient hyponatremia occurred 1-3 days after lesioning and returned to normal by day 7 which corresponds to the timing of the second phase of the triphasic response in rats. hyponatremia was accompanied by vasopressin levels inappropriate for the plasma sodium level, inappropriately concentrated urine, water retention, and natriuresis.(ABSTRACT TRUNCATED AT 250 WORDS)
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ranking = 1
keywords = diabetes insipidus, insipidus, diabetes
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9/37. Transient lymphocytic panhypophysitis associated with SIADH leading to diabetes insipidus after glucocorticoid replacement.

    A 52-year-old man presented with vomiting, general fatigue and hyponatremia. His symptoms and signs were consistent with the syndrome of inappropriate secretion of antidiuretic hormone (SIADH). Endocrine studies revealed hypopituitarism and administration of hydrocortisone resulted in a marked polyuria. The patient was diagnosed as masked diabetes insipidus. The lymphocytic hypophysitis was also diagnosed on the basis of MRI findings and anti-pituitary antibody. Six months later, these abnormalities disappeared. diabetes insipidus may exist in a case of hyponatremia due to contrastive SIADH. Such patients may recover spontaneously and careful follow-up is required, avoiding a long-term treatment by monotonous continuation of hormonal replacement.
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ranking = 1.0392826955407
keywords = diabetes insipidus, insipidus, diabetes
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10/37. Novel mutant vasopressin-neurophysin II gene associated with familial neurohypophyseal diabetes insipidus.

    We describe a novel missense mutant of arginine vasopressin (AVP)-dependent neurohypophyseal diabetes insipidus in an autosomal dominant family. A 54-year-old woman was admitted to our hospital because of thyroidectomy for thyroid cancer. After thyroidectomy she was found to have hypernatremia and polyuria and polydipsia both of which had been present from childhood. She had no obstructive hydronephrosis. Her father, father's younger sister and her third son also had polyuria and polydipsia. Basal plasma AVP concentration at normal plasma osmolality was normal but did not respond to increased plasma osmolality despite hyperosmolality during infusion of hypertonic saline infusion, indicating that plasma AVP secretion was impaired. Sodium concentration in urine and urine osmolality were low and increased after nasal administration of DDAVP. There was a diminished but bright signal of pituitary posterior gland on magnetic resonance T1 weighted image. Molecular genetic analysis demonstrated that the patient and her son had a single heterozygous missense mutation (G-->A) at nucleotide 1829 in 1 AVP allele, yielding an abnormal AVP precursor with lacking Glu-47 in its neurophysin II moiety. The abnormal AVP precursor may be related to the impaired AVP secretion.
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ranking = 1
keywords = diabetes insipidus, insipidus, diabetes
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